Garcia Perez M, Jordan D
Department of Physiology, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.
Auton Neurosci. 2001 Jan 14;86(3):183-91. doi: 10.1016/S1566-0702(00)00252-6.
It has previously been demonstrated in several species that stimulation of myelinated vagal efferent fibres evokes slowing of heart rate and atrio-ventricular (A-V) conduction and a decreased ventricular contractility but recruitment of non-myelinated fibres did not further increase the response. Only in rabbits was a significant bradycardia evoked on recruiting non-myelinated fibres. However, if stimulating myelinated fibres produced a near maximal response, then effects of further activation of non-myelinated fibres may have been missed. Indeed, selective stimulation of non-myelinated fibres alone now has been shown to evoke a slowing of heart rate independent of the effects of myelinated fibres. In the present study we tested in rabbits whether selective stimuli are also capable of slowing A-V conduction and changing ventricular contractility. In rabbits pretreated with the beta 1-adrenoceptor antagonist atenolol, ECG, arterial blood pressure, left ventricular pressure and dP/dt were recorded before and during stimulation of non-myelinated vagal efferent fibres using an anodal block technique (J. Physiol. 273 (1977) 539). R-R interval and A-V conduction times were computed off-line. Stimulation of non-myelinated vagal fibres increased R-R interval by 97.7 +/- 18.8 ms from a baseline of 315.3 +/- 7.7 ms, increased A-V conduction time by 9.9 +/- 1.1 ms from a baseline of 81.9 +/- 3.1 ms and decreased left ventricular dP/dtmax by 2486 +/- 362 mmHg s-1 from a baseline of 11,186 +/- 795 mmHg s-1. When hearts were paced at a rate about 10% higher than normal, A-V conduction time still increased by 13.3 +/- 1.9 ms from a baseline of 104.2 +/- 3.6 ms and dP/dtmax still fell by 2300 +/- 188 mmHg s-1 from a baseline of 11,200 +/- 777 mmHg s-1. Ganglionic blockade with hexamethonium (15-20 mg kg-1) always abolished the evoked increases in A-V conduction time, whilst there was still an increase in R-R interval in seven of the 12 animals tested. The data demonstrate that non-myelinated vagal efferent fibres can modulate chronotropic, dromotropic and inotropic actions on the heart.
此前在多个物种中已证实,刺激有髓迷走神经传出纤维会导致心率减慢、房室(A-V)传导减慢以及心室收缩力降低,但募集无髓纤维并不会进一步增强这种反应。只有在兔子中,募集无髓纤维时会诱发显著的心动过缓。然而,如果刺激有髓纤维产生了接近最大的反应,那么无髓纤维进一步激活的效应可能就被忽略了。事实上,现在已表明单独选择性刺激无髓纤维可诱发心率减慢,且与有髓纤维的效应无关。在本研究中,我们在兔子身上测试了选择性刺激是否也能够减慢房室传导并改变心室收缩力。在预先用β1肾上腺素能受体拮抗剂阿替洛尔处理的兔子中,在使用阳极阻滞技术刺激无髓迷走神经传出纤维之前和期间记录心电图、动脉血压、左心室压力和dP/dt(《生理学杂志》273 (1977) 539)。离线计算R-R间期和房室传导时间。刺激无髓迷走神经纤维使R-R间期从基线的315.3±7.7毫秒增加了97.7±18.8毫秒,使房室传导时间从基线的81.9±3.1毫秒增加了9.9±1.1毫秒,并使左心室dP/dtmax从基线的11,186±795毫米汞柱/秒降低了2486±362毫米汞柱/秒。当心脏以比正常心率高约10%的速率起搏时,房室传导时间仍从基线的104.2±3.6毫秒增加了13.3±1.9毫秒,dP/dtmax仍从基线的11,200±777毫米汞柱/秒下降了2300±188毫米汞柱/秒。用六甲铵(15 - 20毫克/千克)进行神经节阻滞总是能消除诱发的房室传导时间增加,而在12只受试动物中有7只的R-R间期仍有增加。数据表明,无髓迷走神经传出纤维可调节心脏的变时、变传导和变力作用。